Use of Interleukin (IL)-34 to Treat Retinal Inflammation and Neurodegeneration

Interleukin (IL)-34 is a homodimer that is produced mainly by keratinocytes, neuronal cells and regulatory T cells (Tregs). It is believed to play important roles in chronic inflammation and the homeostasis of microglia. Currently, there is no effective treatment for many types of retinal degeneration. An improved treatment of autoimmune uveitis is also needed, as current uveitis treatment primarily uses steroidal anti-inflammation medication, which may produce significant unwanted side effects in long-term use.

Ex-vivo Production of Regulatory B-Cells for Use in Auto-immune Diseases

Regulatory B-cells (Breg) play an important role in reducing autoimmunity and reduced levels of these cells are implicated in etiology of several auto-inflammatory diseases. Despite their impact in many diseases, their physiological inducers are unknown.  Given that Bregs are a very rare B-cell, identifying factors that promote their development would allow in vivo modulation of Breg levels and ex-vivo production of large amounts of antigen-specific Bregs to use in immunotherapy for auto-inflammatory diseases.
 

Interleukin 24 (IL-24) to treat inflammatory diseases

Proinflammatory T-helper 17 cells (Th17) play important roles in host immune defense against infection, but uncontrolled activation of these cells, known as the Th17 response, may cause autoimmune and autoinflammatory diseases (uveitis, multiple sclerosis, rheumatoid arthritis, and Crohn’s disease) through the effects of Th17 lineage cytokines (such as, IL-17F, IL-22 and GM-CSF). Importantly, IL-17A (a proinflammatory cytokine) represses other Th17 lineage cytokines by upregulating the regulatory cytokine IL-24.

Camel VHH Nanobodies Bind the S2 Subunit of SARS-CoV-2 and Broadly Neutralize Variants including Omicron

Since its emergence in 2019, COVID-19 infected over 600 million people and over 6 million people have died from the disease. COVID-19 is an infectious disease caused by the SARS-CoV-2 virus. Neutralizing antibodies have been developed to bind to the receptor binding domain (RBD) on the spike (S) protein. Blocking the interaction of the RBD and the ACE2 receptor, is critical in neutralizing the virus. However, the S2 subunit, is also critical for viral infection and entry into human cells.

Humanized Monoclonal Antibodies Specific Against Human Soluble Tissue Factor (hsTF) as Diagnosis, Prevention and Therapeutic Agents for Thrombosis

Summary:

The National Cancer Institute (NCI) seeks research co-development partners and/or licensees for a novel humanized monoclonal antibody (58B3) that selectively targets a newly identified soluble Tissue Factor (sTF) to diagnose, prevent and treat pathological thrombosis associated with inflammation, viral/bacterial infection, sepsis and cancer – without affecting normal hemostasis.

Novel Human Immunogenic Epitopes of the Human Endogenous Retrovirus ERVMER34-1

Summary:

The National Cancer Institute (NCI) seeks research co-development partners and/or licensees for the clinical translation of novel peptide-based therapeutic cancer vaccines derived from ERVMER34-1, a human endogenous retrovirus (HERV) antigen, offering a unique opportunity to address a significant unmet need in the treatment of various carcinomas.

Identification and Characterization of HLA-A24 Agonist Epitopes of MUC1 Oncoprotein

Summary:

The National Cancer Institute (NCI) seeks co-development partners and licensees for a human cytotoxic T lymphocyte agonist epitope from the C-terminal subunit of mucin 1 (MUC1-C), which can be used as a peptide, polypeptide (protein), in a cancer vaccine or T-cell targeted therapy to target many tumor types.

Methods of Detecting Loss of Heterozygosity and Damaging Mutations in Immune-Related Genes Using Liquid Biopsies

Summary: 
The National Cancer Institute (NCI) seeks co-development partners and/or licensees for a liquid biopsy diagnostic assay capable of detecting loss of heterozygosity (LOH) and somatic mutations in genes important for antigen processing and presentation and interferon-γ response pathways.